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http://purl.uniprot.org/citations/23172686http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23172686http://www.w3.org/2000/01/rdf-schema#comment"Silent information regulator T1 (SirT1) is linked to longevity and negatively controls NF-κB signaling, a crucial mediator of survival and regulator of both osteoclasts and osteoblasts. Here we show that NF-κB repression by SirT1 in both osteoclasts and osteoblasts is necessary for proper bone remodeling and may contribute to the mechanisms linking aging and bone loss. Osteoclast- or osteoblast-specific SirT1 deletion using the Sirt(flox/flox) mice crossed to lysozyme M-cre and the 2.3 kb col1a1-cre transgenic mice, respectively, resulted in decreased bone mass caused by increased resorption and reduced bone formation. In osteoclasts, lack of SirT1 promoted osteoclastogenesis in vitro and activated NF-κB by increasing acetylation of Lysine 310. Importantly, this increase in osteoclastogenesis was blocked by pharmacological inhibition of NF-κB. In osteoblasts, decreased SirT1 reduced osteoblast differentiation, which could also be rescued by inhibition of NF-κB. In further support of the critical role of NF-κB signaling in bone remodeling, elevated NF-κB activity in IκBα(+/-) mice uncoupled bone resorption and formation, leading to reduced bone mass. These findings support the notion that SirT1 is a genetic determinant of bone mass, acting in a cell-autonomous manner in both osteoblasts and osteoclasts, through control of NF-κB and bone cell differentiation."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.org/dc/terms/identifier"doi:10.1002/jbmr.1824"xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/author"Edwards J.R."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/author"Ono K."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/author"Moore M.M."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/author"Mundy G.R."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/author"Elefteriou F."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/author"Yull F.E."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/author"Fleming N."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/author"Connelly L."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/author"Perrien D.S."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/author"Lwin S.T."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/author"Nyman J.S."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/name"J Bone Miner Res"xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/pages"960-969"xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/title"Silent information regulator (Sir)T1 inhibits NF-kappaB signaling to maintain normal skeletal remodeling."xsd:string
http://purl.uniprot.org/citations/23172686http://purl.uniprot.org/core/volume"28"xsd:string
http://purl.uniprot.org/citations/23172686http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23172686
http://purl.uniprot.org/citations/23172686http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23172686
http://purl.uniprot.org/uniprot/#_A0A0G2JGK6-mappedCitation-23172686http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23172686
http://purl.uniprot.org/uniprot/#_A0A077S2U6-mappedCitation-23172686http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23172686
http://purl.uniprot.org/uniprot/#_A7MCT8-mappedCitation-23172686http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23172686
http://purl.uniprot.org/uniprot/#_F6YAQ3-mappedCitation-23172686http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23172686